Electrolyte balance in critically ill patients

WATER AND ELECTROLYTES BALANCE

IN ICU

SAMIR EL ANSARYICU PROFESSOR

AIN SHAMSCAIRO

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Objectives

• Explain in flow chart form how the rates of sodium and water excretion are affected by:

–Drinking isotonic saline

–Partial constriction of a single renal artery

–Profuse sweating

Describe the effects of drinking water, or the intravenous infusion of saline solutions of different osmolalities on the

volumes and osmolalities of various body fluid spaces.

EC vol. IC vol. EC osm. IC osm.

Isotonic saline

Water

Hypertonic Saline

Hypotonic saline

1.

Sodium Reabsorption

Sodium balance

Most NaCl intake added during food preparation

Sweat output depends on body temperature

Urine output of NaCl is regulated by blood pressure

Water balance

Metabolically produced by oxidation of H-containing nutrients

Insensible loss: expiration of 37 saturated air, evaporation through skin (different from sweat)

Urine output regulated by vasopressin (antidiuretic hormone ADH)

Juxtaglomerular apparatus

Macula densa: specialized cells in wall of distal tubule

Juxtaglomerular cells (Granular cells): contain renin, sympathetic nerves

Forces of filtration

Substance X: filtered & entirely secreted (rare)

Substance Y: filtered & partially reabsorbed (Na+, K+, water)

Substance Z: filtered & entirely reabsorbed (glucose, amino acids)

Kidney handling of various substances

Water LoadingDrink Water

Plasma Osmolality

Activation of osmoreceptors inanterior hypothalamus

ADH secretion from Post. Pituitary

Water permeability in late DT and CT

Water Reabsorption

Urine Osmolality Urine Volume

Water Deprivation Drink Water

Plasma Osmolality

Activation of osmoreceptors inanterior hypothalamus

ADH secretion from Post. Pituitary

Water permeability in late DT and CT

Water Reabsorption

Urine Osmolality Urine Volume

4.

Review: Hormones of Water and Sodium Regulation

• Angiotensin-II

• Anti-diuretic hormone/vasopressin/AVP

• Aldosterone

• Atrial natriuretic peptide (ANP)

Reninangiotensinaldosteronesystem

Reninangiotensinaldosteronesystem on Na+

excretion

Macula densa: specialized cells in wall of distal tubule

Juxtaglomerular cells (Granular cells): contain renin, sympathetic nerves

Juxtaglomerular apparatus

Mesangial cells.

1.

2.

3. Pressure (less stretch)

Decreased NaCl sensing

Sympathetic NS

RENIN

Actions of aldosterone

Aldosterone actions: Na+ channel activity, K+

channel activity, Na+/K+ ATPase pumpNote: large Na+, K+ shows high concentration & vice versa

ANP actions:

1. Na+ reabsorption from deep medullary collecting duct

2. glomerular filtration rate

Both actions Na+ excretion

Atrialnatriuretic

peptide on Na+

excretion

Vasopressin (ADH) release & actions

Vasopressin release stimulated by:

1.slight (1%) increase in plasma osmolality

2.large (~10-15%) reduction in plasma volume

Vasopressin action:

Increases permeability of collecting duct to water

Vasopressin (ADH) release & actions

Renal medulla

has osmotic gradient from 300 mOsm/kg at cortical border to 1200 mOsm/kg at deepest part of medulla

ADH levels collecting duct

permeability water reabsorption urine volume with osmolality

Diabetes Insipidus

• Loss of ADH secretion or insensitivity of kidneys to ADH

• Large severely dilute amounts of urine

• Increased intake of water

• Danger lies in hyponatremia and ultimate central nervous system edema and death.

Types of Diabetes Insipidus

• Central– Damage to hypothalamus – no ADH

• Nephrogenic– Kidneys cannot respond to ADH

– Usually genetic (rare) 90% cases due to V2receptor mutation, 10% due to Aquaporinmutation.

Types of Diabetes Insipidus

• Dipsogenic–Damage to thirst center – making patient

abnormally thirsty

• Gestational–During pregnancy women produce

vasopressinase which breaks down ADH, increasing urine output.

ADH Mechanism of Action

Receptor binds, causes vesicles to fuseand insert aquaporins (water channels)

into the membrane.

5.

How to test for it?

• Water deprivation test– If water deprivation results in dilute voluminous

urine, then cause is likely not dipsogenic (but central or nephrogenic)

• Desmopressin test (ADH analog)– Central and Gestational respond to this treatment

– Nephrogenic does not

• If kidneys are insensitive, then they won’t respond.

SIADH (syndrome of inappropriate ADH

secretion)

• Excessive ADH secretion• Not “turned off” by drop in osmolality from

drinking water and water retention.

• Hyponatremia is also the main concern

• Causes– Head trauma

– Ectopic lung tumor (secretes ADH).

– Treatment – water deprivation or removal of tumor

Water transport & vasopressin actions

Sweat is hypotonic (i.e. osmolality < plasma)

Sweating without water replacement

Regulation of thirstSensation of thirst stimulated by:1. 1% osmolality2. >10-15% blood volume3. angiotensin II

Isotonic saline

Extracellular volume

Blood pressure

Renin, angiotensinaldosterone

Sympathetic NS

Sodium excretion

Plasma osmolality

Atrial Natriuretic peptide

ADH secretion

Water excretion

-

Extracellular fluid volume Extracellular osmolality

thirst ADH secretion

Water reabsorption

Water excretion

Sweating on salt & water excretion

Contstriction of renal artery

Afferent arteriole pressure

RENIN

Angiotensin-II

Aldosterone

Increase Na+

reabsorption

Plasma osmolality

vasoconstriction

ADH

Salt and water retention

Water excretion

Extracellular & vascular volume

Increased systemic blood pressure

GFR

Sodium filtered

Sodium excreted

What is renal hypertension? (renovascular hypertension)

BEFORE

AFTER

1) “ESSENTIAL” HYPERTENSION

-no specific cause-body unable to regulate blood pressure-systolic BP >140, diastolic > 90mmHg -Managed with meds, diet, and fluid regulation(ACE inhibitors/diuretics)

2) SECONDARY HYPERTENSION

-most common cause isrenal artery stenosis due to atherosclerosis.-usually diagnosed after long-standingHTN becomes unmanageable. -results in very high BP-systolic >200, diastolic >100 mmHg. -decreased RBF (sensed as a drop in BP) results in increases in RENIN, thus causing further peripheral vasoconstriction, sodium/water retention and increases in BP.

PLAQUES ORFIBROSIS

Isotonic expansion of renovascularhypertension

Renin angiotensin aldosterone - high Both RVH and Aldosteronism resultin hypertension

AldosteroneCase E2

“hypertensive 43 y/o F”

Case E5“nausea, weakness,wt. loss 32 y/o M”

Tonicity TonicityVolumeVolume

[Na+] (144)[K+] (2.9)

[Na+] (123)[K+] (6.4)

HTN Bun/Cr = 26

Differentials

Isotonic Expansion

-hypertension-renovascular hypertension-aldosteronism

Hypotonic Contraction

-chronic salt loss w/water replac.-diuretic use (chronic)

-Addison’s disease

Diagnosis Conn’s syndromePrimary aldosteronism

(elevated Aldosterone/low renin)

Treatment/Tests

Surgical removal of tumorSpironolactone

Addison’s disease(low Na, high K, acidosis,

low glucose, tanned appearance)

Measure [corticosteroid]

Excessive diuretic use (hypotonic contraction)?Excessive loop or thiazide diuretic

↓ Na+ reabsorption DCT

↓ plasma osmolality

↓ ADH

↑ water excretion

↑ K+ excretion/hypokalemia

(isotonic)

↓ vascular volume ↑ RAA

↑ Na reabsorption(at principal cell)

↑ H excretion

Metabolic alkalosis

(when > 10%)

↑ ADH

↑ water retention

hyponatremia

Addison’s disease (hypotonic contraction)?

↓ aldosterone/glucocorticoids

↓ Na+ reabsorption (principal cell)

↓ plasma osmolality

↓ ADH

↑ water excretion

↓ K+ excretion/hyperkalemia

(isotonic)

↓ vascular volume

↓ H+ excretion/Metabolic acidosis

(when > 10%)

↑ ADH

↑ water retention

hyponatremia

(osmotic response)

hypoglycemia

(pressure response)

Anti-diuretic hormone

Case E3“head trauma MVA”

Case E6“SOB, wt. loss, hemoptysis

and wheezing”

Tonicity TonicityVolume Volume

[Na+] (162)[K+] (3.8)

[Na+] (110)[K+] (4.5)

Bun/Cr = 5.7U[80]mOsmolhemoconcentration

P[230]mOsmolU[496]mOsmol

Differentials

Hypertonic Contraction

-dehydration – bun? Urine vol?-acute renal failure – urine too dilute-diabetes insipidus

Hypotonic Expansion

-polydipsia – [urine]?-Addison’s disease -SIADH

Diagnosis Diabetes Insipidus (low ADH)High plasma osmolality,

Low urine osmolality

Treatment/Tests

Desmopressin test(response – neurogenic)(no response – nephrogenic)

SIADH (high ADH)Low plasma osmolalityHigh urine osmolality

Chest X-rayRemove ADH secreting tumor

water loss > salt loss salt loss > water loss

SIADH (hypotonic expansion) vs. Diabetes Insipidus (hypertonic contraction)

↑ Anti-diuretic hormone ↓

↑ thirst – activation ofhypothalamic

osmoreceptors

↓ Na reabsorption↓ K excretion

↓ renin-angiotensin-aldosterone

↑ MAP

↑ water reabsorptionat principal cells

↑ vascular volume

↑ water excretion

↓ MAP

↓ vascular volume

hyponatremia

Water retention + Na excretion explains low plasma osmolalityand relatively increased urine osmolality (SIADH)

↑ ANP

↑ renin-angiotensinaldosterone

↑ Na reabsorption↑ K excretionhypernatremia

Global Critical Carehttps://www.facebook.com/groups/1451610115129555/#!/groups/145161011512

9555/ Wellcome in our new group ..... Dr.SAMIR EL ANSARY

GOOD LUCK

SAMIR EL ANSARY

ICU PROFESSOR

AIN SHAMS

CAIRO

[email protected]